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Biomedical subjects

Robert M Genta

Publications and source records attributed to Robert M Genta.

At least 19 recordsLinked to original sources
PubMed2007

Napoleon Bonaparte's gastric cancer: a clinicopathologic approach to staging, pathogenesis, and etiology.

BACKGROUND: Numerous hypotheses on the cause of Napoleon Bonaparte's death have been proposed, including hereditary gastric cancer, arsenic poisoning, and inappropriate medical treatment. We aimed to determine the etiology and pathogenesis of Napoleon's illness by a comparison of historical information with current clinicopathologic knowledge. INVESTIGATIONS: Evaluation of Napoleon's clinical history, original autopsy reports, and of historical documents. The clinicopathologic data from 135 gastric cancer patients were used for comparison with the data available on Napoleon. DIAGNOSIS: At least T3N1M0 (stage IIIA) gastric cancer. Napoleon's tumor extended from the cardia to the pylorus (>10 cm) without infiltration of adjacent structures, which provides strong evidence for at least stage T3. The N1 stage was determined by the presence of several enlarged and hardened regional (perigastric) lymph nodes, and the M0 stage by the absence of distant metastasis. Analysis of the available historical documents indicates that Napoleon's main risk factor might have been Helicobacter pylori infection rather than a familial predisposition. CONCLUSIONS: Our analysis suggests that Napoleon's illness was a sporadic gastric carcinoma of advanced stage. Patients with such tumors have a notoriously poor prognosis.

Famous Persons↗
PubMed2006

Assessing risks for gastric cancer: new tools for pathologists.

Although the Sydney Systems (original and updated) for the classification of gastritis have contributed substantially to the uniformity of the reporting of gastric conditions, they lack immediacy in conveying to the user information about gastric cancer risk. In this review, we summarize the current understanding of the gastric lesions associated with an increased risk for cancer, and present the rationale for a proposal for new ways of reporting gastritis. In addition to the traditional histopathological data gathered and evaluated according to the Sydney System rules, pathologists could add an assessment expressed as grading and staging of the gastric inflammatory and atrophic lesions and integrate these findings with pertinent laboratory information on pepsinogens and gastrin levels. Such an integrated report could facilitate clinicians' approach to the management of patients with gastric conditions.

Biopsy↗
PubMed2006

Helicobacter pylori infection in patients with celiac disease.

BACKGROUND AND AIMS: Patients with Helicobacter pylori gastritis are more likely to have increased duodenal intraepithelial lymphocytes (IEL); this can be reversed by H. pylori eradication. We hypothesized that: (1) H. pylori-infected celiac disease (CD) patients could have different clinicopathological features from noninfected subjects; and (2) the histopathological responses to a gluten-free diet could be different in H. pylori-infected and noninfected patients. METHODS: Duodenal and gastric biopsies obtained from 80 adults with histologically and serologically confirmed CD before and after 12-18 months of a gluten-free diet were retrospectively evaluated. Gastritis was classified and scored according to the Updated Sydney System; duodenal biopsies were classified using both the Marsh-Oberhuber and a simplified classification proposed by our group. RESULTS: At baseline, 30 patients had H. pylori infection and 50 did not; at follow-up five new infections were detected. Fifteen patients (3 H. pylori-positive and 12 negative) had lymphocytic gastritis. At baseline, a greater proportion of H. pylori-negative patients had severe villous atrophy (p < 0.01), but milder forms were more prevalent in H. pylori-positive patients (p < 0.01). After a gluten-free diet, significant improvement occurred in all duodenal features (p < 0.001), irrespective of H. pylori status; gastric variables did not change, except for lymphocytic, which resolved in 2 infected and 10 noninfected patients. CONCLUSIONS: The clinical features of CD patients are unrelated to H. pylori gastritis, and a gluten-free diet is equally effective in infected as in uninfected patients. The higher prevalence of milder duodenal lesions in CD patients with H. pylori infection suggests that lymphocytosis induced by H. pylori gastric infection becomes less obvious as profound inflammatory and structural changes alter the mucosal architecture. This study also provides further support for a pathogenetic relationship between CD and lymphocytic gastritis.

Adult↗
PubMed2006

Association between gastric atrophy and Helicobacter pylori infection in Japanese children: a retrospective multicenter study.

The purpose of this study was to determine whether Helicobacter pylori infection and mucosal inflammation result in gastric atrophy in Japanese children. A total of 196 patients ages 1-16 years were retrospectively studied: 131 patients were infected with H. pylori and 65 patients were uninfected. Antral (n = 196) and corpus biopsy specimens (n = 70) were investigated based on the Updated Sydney system. In both the antrum and corpus, H. pylori-infected patients showed significantly higher degrees of inflammation and activity of gastritis, compared with noninfected patients. The prevalence of grade 2 or 3 atrophy in the antrum was 10.7% in H. pylori-infected patients and 0% in the noninfected patients (P < .01) and in corpus 4.3% and 0%, respectively (P = .20). The frequency of intestinal metaplasia in the 2 study groups was 4.6% and 4.6% in the antrum and 0% and 4.2% in the corpus, respectively. Among H. pylori-infected patients, the antrum showed significantly higher degrees of H. pylori density, inflammation and activity of gastritis, and atrophy than the corpus. In the antrum, atrophy was significantly correlated with activity, whereas in the corpus, atrophy correlated with H. pylori density, inflammation, and activity. H. pylori-induced gastric inflammation can cause atrophy in Japanese children, predominantly in the antrum. It remains to be determined whether H. pylori-infected children with gastric atrophy are at increased risk for gastric cancer.

Adolescent↗
PubMed2006

Systemic rheumatoid vasculitis: a review.

OBJECTIVES: To review the most recent information on the incidence, clinical course, pathology, pathogenesis, diagnosis, and treatment of rheumatoid vasculitis (RV), including the still scanty data on the use of biologics. METHODS: PubMed and MEDLINE databases (1950-2006) were searched for the key words "vasculitis" and "rheumatoid arthritis"; and "rheumatoid arthritis" and "extra-articular manifestations." All relevant articles in English and French were reviewed. Additional words used in follow-up research include "anti-TNF," "rituximab," "IL-1 receptor antagonists," and "CTLA-4 Ig," all in conjunction with "vasculitis." Pertinent secondary references were also retrieved. RESULTS: RV is an inflammatory condition of the small- and medium-sized vessels that affects a subset of patients with established rheumatoid arthritis (RA) (approximately 1 to approximately 5%). It has a vast array of clinical manifestations with a predilection for the skin (peripheral gangrene, deep cutaneous ulcers) and the peripheral nervous system (mononeuritis multiplex). Because of the lack of specific signs and symptoms, the diagnosis relies on the exclusion of other causes of similar lesions (diabetes, atherosclerosis, drug reactions, infection, neoplasias) and, ideally, on the histopathological demonstration of necrotizing vasculitis. Despite the availability of a host of promising new drugs for the treatment of RA, no clinical trials have tested their efficacy in RV; therefore, its management remains largely empirical. CONCLUSIONS: Although RV has apparently been decreasing over the last 2 decades, possibly as a consequence of the more energetic approach to the management of RA currently used, it remains an important complication of RA that needs to be promptly recognized and treated.

Arthritis, Rheumatoid↗
PubMed2006

The gastric mucosa in gastric cancer patients in a low-incidence area.

BACKGROUND AND AIMS: Atrophic gastritis, intestinal metaplasia, and pyloric metaplasia are frequent precursors of noncardial intestinal-type gastric adenocarcinoma in populations in which both gastric cancer and Helicobacter pylori infection are common. We hypothesized that such lesions would be less prevalent in European gastric cancer patients. METHODS: Slides from patients who underwent gastrectomy for adenocarcinoma between 1997 and 2004 were reviewed. Tumors were categorized as intestinal or diffuse; non-neoplastic mucosa was evaluated for gastritis, atrophy, intestinal metaplasia and pyloric metaplasia. RESULTS: We studied 81 patients: 48 Swiss (mean age 68.5 years); 17 Italians (mean age 67.8 years); and 16 Iberians (mean age 54.8 years; P<0.001). Twelve tumors were proximal (all intestinal type), 12 in the corpus (six intestinal-type), and 57 antral (30 intestinal type). Patients with diffuse cancers were younger than those with intestinal type (P<0.05). Nineteen patients (23.4%) had a normal stomach; 30% of T1 tumors and 90% of T4s arose in a normal stomach (P<0.02). H. pylori gastritis was found in 47 patients (58%); they did not differ in age, sex, national origin, cancer location or type from those without gastritis. Intestinal metaplasia correlated with H. pylori gastritis (P=0.002). Pyloric metaplasia was infrequent and limited to rare microfoci. CONCLUSIONS: A quarter of the patients had a normal stomach, and pyloric metaplasia was distinctly uncommon. Approaches to prevention and early detection of gastric cancer based on bioptic or serological demonstration of atrophy and metaplasia could overlook at least 25% of the people at risk in certain populations and may need to be adapted to local conditions.

Adenocarcinoma↗
PubMed2005

[Human error, diabolical perseverance].

Medical error is a subject that receives increasing attention from physicians, legislators and attorneys. Taking the lead from a personal event in the author's career, the article focuses on errors in the practice of anatomic pathology. It discusses the difficulties of objectively separating true diagnostic mistakes from the great variability of informed opinions that exists in pathology; such variability makes the definition of error particularly arduous. Some of the possible causes of diagnostic errors and ways to deal with their potentially disastrous consequences are also discussed.

Humans↗
PubMed2005

Staging and grading of chronic gastritis.

Chronic gastritis is an inflammatory condition of the gastric mucosa that may include structural alterations of the glandular compartment. The semiquantitative scoring systems advocated in the Sydney Systems and the subsequent Atrophy Club Guidelines remain essential for the recognition of the spectrum of the lesions detectable in gastric inflammatory disease. Most practicing pathologists, however, find them too cumbersome to use in their routine diagnostic activities. In this article, we propose a reporting system for chronic gastritis in staging and grading. Staging would convey information on the topography and extension of the gastric atrophic changes, whereas grading should represent the semiquantitative assessment of the combined severity of both mononuclear and granulocytic inflammation. This system could offer gastroenterologists a more immediate perception of the overall condition of the gastric mucosa while also providing useful information about gastric cancer risk.

Atrophy↗
PubMed2005

Differential diagnosis of reactive gastropathy.

Reactive or chemical gastropathy is the constellation of endoscopic and histological changes caused by chemical injury to the gastric mucosa. Its diagnosis rests on the histopathological demonstration of nonspecific elementary lesions that may occur simultaneously or separately in different degrees and various proportions. These lesions include foveolar hyperplasia, interfoveolar smooth muscle fibers, erosions, edema, and hyperemia, in the absence of significant inflammation. Their respective occurrence in a set of gastric biopsies can be placed on a spectrum of diagnostic certainty that is never absolute because each of such changes can and does occur in other conditions. Although a correlation between histological evidence of chemical gastropathy and clinical manifestations, particularly risk of bleeding, is yet to be documented, reporting the suspicion of drug-induced gastric damage may help clinicians to identify patients that might benefit from change, reduction, or discontinuation of certain medications.

Algorithms↗
PubMed2005

Non-invasive neoplasia of the stomach.

Invasive gastric cancer is the final step of a cascade of genomic and phenotypic changes, which have been defined as multistep oncogenesis. This process includes a continuum of progressively dedifferentiated phenotypes, which may result in a biologically new (i.e., nuepsilonomega = neo) cell characterized by autonomous, potentially metastatic, growth (i.e., pilambdaalphazetaomega = plasia). The clinico-pathological characterization of the advanced gastric precancerous lesions has important implications for both primary and secondary cancer prevention. The WHO agency has recently redefined dysplasia as intraepithelial [i.e., non-invasive neoplasia (NiN)]; such a proposal is consistent with the biological profile of dysplasia, which shares with invasive cancer some significant molecular attributes. Long-term follow-up studies have demonstrated that, in the natural history of gastric cancer, NiN precedes invasive adenocarcinoma. In this review, the morphological features of gastric NiN are described, also illustrating differences and similarities between the current and the previously adopted histological diagnostic criteria. The molecular profile of NiN is summarized and the spectrum of the options in the clinical management of gastric NiN are reported.

Disease Progression↗
PubMed2004

Gastroesophageal reflux among different racial groups in the United States.

BACKGROUND & AIMS: White people in the United States are several-fold more affected by esophageal adenocarcinoma than black people. It remains unknown whether this racial discrepancy reflects a higher prevalence of gastroesophageal reflux disease (GERD) symptoms or a higher degree of esophageal damage. METHODS: A cross-sectional survey followed by endoscopy was performed among employees at a VA medical center. The association between race and GERD symptoms and erosive esophagitis was analyzed in logistic regression analyses controlling for demographic, clinical, and histologic variables. RESULTS: A total of 496 of 915 people (54%) returned interpretable questionnaires, and endoscopy was performed in 215 participants. The mean age was 45 years, and 336 (68%) were women. Racial distribution was 43% black, 34% white, and 23% other races. Heartburn occurring at least weekly was reported in 27%, 23%, and 24% of these racial groups, respectively. The age-adjusted prevalence of heartburn or regurgitation was not significantly different among the groups. Erosive esophagitis was found in 50 of 215 participants (23%); 31 of these cases were mild. Only one person had Barrett's esophagus (0.4%). For weekly heartburn or regurgitation, black participants had significantly less frequent erosive esophagitis than white participants (24% vs. 50%; P = 0.03). With multiple adjustments, black participants had a persistently lower risk of esophagitis (adjusted odds ratio, 0.22-0.46; P < 0.001). CONCLUSIONS: White and black people in the United States have a similarly high prevalence of GERD symptoms. However, black people have a lower prevalence of esophagitis for the same frequency of GERD symptoms. Barrett's esophagus was rare in this study, even among those with frequent symptoms.

Adolescent↗